The article referenced in post #1 is an interesting bit of data. It suggests one more potential marker for an uncommon, yet extremely serious in-water occurrence. I would be interested in
@Dr Simon Mitchell 's take on the data, as another CCR diver-anesthesiologist.
As interesting as this study is, one must realize that the "comet score" referred to in the last paragraph is at least two steps removed from the problem. In other words, an increased comet score appears to be correlated with "extravascular lung water", which is fluid that for hydrostatic (and other) reasons has left the circulation and may or may not begin to occupy alveolar space. It is excess water in the pulmonary tissue that marks the onset of pulmonary edema, and fluid in the alveoli themselves with lung consolidation which marks the most severe cases.
Pulmonary edema itself is a simply explained phenomenon: an increased fluid gradient coupled possibly with cellular membrane issues allows water to transit from the circulation to the extravascular space and then possibly accumulate in the lung alveoli, both with predictable effects on oxygen exchange.
But the chain leading to IPE is quite complex. One must examine not only physical gradients but cellular membrane contributors. We have seen suggestions that those with underlying heart disease are less able to tolerate the sudden increase in intravascular volume upon immersion, which creates a pressure gradient. We have seen suggestions that the venous bubbling which accompanies most ascents from depth (with or without symptomatic DCI) can be associated with a rise in various inflammatory markers which may affect cellular membranes. Suggested in the article is a possible contribution from
over-hydration pre-dive. Exertion increases pulmonary artery pressure. Negative inspiratory pressure probably worsens the intra-alveolar hydrostatic gradient.
And therefore, most interesting to me as a CCR diver is the comment about counterlung position. As an anesthesiologist regularly caring for patients with active pulmonary edema, it is routine to apply 5cm water pressure (or more) of "Positive End-Expiratory Pressure" during surgery. This PEEP provides a physical pressure inside the alveoli which may help to prevent worsening of pulmonary edema during the operation, through the simple expedient of a physical factor countering a hydrostatic gradient.
In contrast, during my CCR diving with BMCL, I am acutely aware of the slight negative inspiratory pressure which accompanies horizontal (or much worse: head-down) diving with "min loop volume".
Those divers who experience IPE are relatively small in number and are sometimes found to have occult cardiac or pulmonary abnormalities which may have predisposed them to the problem. However, as this study suggests, IPE can occur even in healthy individuals, typically associated with exertion. It is that fact, coupled with my particular awareness of loop pressure during breathing, that makes this study of interest. I would like, even absent known cardiac disease, to minimize the factors that might contribute to pulmonary edema during a dive. I can try to minimize exertion; I can mitigate gas density with helium; I can perhaps avoid a head up position during ascent. And with this study, I find some ammunition to use against those that constantly preach min loop volume.
Min loop volume can be a great help to buoyancy control during CCR diving. I certainly went to great lengths to reduce the amount of carried lead on my rig to keep my "bubble" as small as possible. But I have gradually increased the amount of gas carried in my JJ counterlungs, and decreased the amount I add to my wing in compensation. With back mounted counterlungs, I can easily feel the difference during breathing, when I no longer have to suck gas around my shoulder to the T-piece when the CL's are very empty. Given my predilection for PEEP in the operating room, that reassures me.
An occurrence during Advanced Wreck training drove this point home hard: deep in the Spiegel Grove, we were transiting from ~110' to 130' to enter the forward engine room. Our route took us down two decks using two sequential vertical trunks about 3' x 3' in size. Once head down, there was no turning around, and the gas in my counterlungs went to the highest point, leaving the bag going around my shoulder to the T-piece completely flat. I could not, or almost not, breathe! Filling my counterlung would have added 4lb or more buoyancy during a descent in a very restricted space.
I was immediately confronted by a potential occurrence I have seen just twice in my 40-year career: "flash pulmonary edema". That occurred when a patient who was breathing normally went into laryngospasm upon removal of the endotracheal tube. Struggling reflexively to inhale for 60 sec against closed vocal cords while medications were administered led 30 minutes later to transient severe pulmonary edema that required reintubation and ventilation with PEEP until the fluid reabsorbed. It occurs
solely due to the onset of a sudden, large negative pressure gradient between the tissue and the adjacent alveoli.
While my own vocal cords were open, I
could not breathe. I dared not try and suck hard to pull gas "around the corner", and maybe risk flash pulmonary edema. I considered going to my bailout necklace. But the trunk was only 10 feet long between each deck, and it was simply easier to just stop breathing until I descended another five feet, exited and rotated horizontal at the next deck. Problem averted. A backup fix had been right at hand. But the lesson was never forgotten. While complete obstruction with BMCL is rare, a negative inspiratory pressure with min loop volume is common. I don't like that.
This study's tiny finding of "comet score 15.1 with BMCL" vs "4.2 comet score with anterior lungs" at rest, and estimated increase in pulmonary artery pressure during exercise of 13mm with anterior CL's vs 17 mm with BMCL adds to my prejudice regarding the possible contribution of loop pressure to the development of IPE, once you add all the other contributing factors. I think the issue is far too complex to make positive vs negative inspiratory pressure the "smoking gun" for IPE. But I'm betting that carrying more loop volume (especially when head down) may help eliminate one contributor for those of us with BMCL. It's one reason why my next look-see for a new toy may be the Choptima.
www.mayoclinic.org
www.ncbi.nlm.nih.gov
